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From the MRI Unit (Drs. Rugg-Gunn, Boulby, Symms, and Duncan), National Society for Epilepsy and Department of Clinical and Experimental Epilepsy, and Department of Neuroinflammation (Dr. Barker), Institute of Neurology, University College London, and Centre for Neuroimaging Sciences (Dr. Barker), Institute of Psychiatry, London, UK.
Address correspondence and reprint requests to Prof. J.S. Duncan, National Society for Epilepsy, Chalfont St. Peter, Gerrards Cross, Bucks SL9 0RJ, UK; e-mail: j.duncan{at}ion.ucl.ac.uk
Objectives: To examine the cerebral structure of 14 patients with partial seizures and acquired lesions, 20 patients with malformations of cortical development (MCDs), and 45 patients with partial seizures and normal conventional MRI using whole-brain T2 mapping and statistical parametric mapping (SPM).
Methods: T2 maps were calculated, and individual patients were compared with a group of 30 control subjects using SPM.
Results: T2 mapping and objective voxel-by-voxel statistical comparison identified regions of increased T2 signal in all 14 patients with acquired nonprogressive cerebral lesions and partial seizures. In all of these, the areas of increased T2 signal concurred with abnormalities identified on visual inspection of conventional MRI. In 18 of 20 patients with MCDs, SPM detected regions of increased T2 signal, all of which corresponded to abnormalities identified on visual inspection of conventional MRI. In addition, in both groups, there were areas that were normal on conventional imaging, which demonstrated abnormal T2 signal. Voxel-by-voxel statistical analysis identified increased T2 signal in 23 of the 45 patients with cryptogenic focal epilepsy. In 20 of these, the areas of increased T2 signal concurred with epileptiform EEG abnormality and clinical seizure semiology. Group analysis of MRI-negative patients with electroclinical seizure onset localizing to the left and right temporal and left and right frontal regions revealed increased T2 signal within the white matter of each respective lobe.
Conclusions: T2 mapping analyzed using statistical parametric mapping was sensitive in patients with malformations of cortical development and acquired cerebral damage. Increased T2 signal in individual and grouped MRI-negative patients suggests that minor structural abnormalities exist in occult epileptogenic cerebral lesions.
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the January 25 issue to find the title link for this article.
Supported by Action Research and the Gwyneth Forrester Trust (F.J.R.-G., P.A.B.) and the Multiple Sclerosis Society of Great Britain and Northern Ireland (G.J.B.). The Glaxo Wellcome scanner and the MRI unit are supported by the National Society for Epilepsy.
Received February 27, 2004. Accepted in final form October 7, 2004.
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